Exercise Acclimation but Not Thermal Area Alters the Cytokine Response to Exertional Heat Stroke

Our group has previously established a model of exertional heat stroke (EHS) that displayed a unique cytokine profile, where cytokines classically involved in the innate immune response were blunted and moved earlier in time compared to passive heat stroke (PHS) models. Limitations in the experimental design may have inadvertently led to this finding. Our objective was to account for these limitations and identify the source of the blunted cytokine response. Acclimation sessions (mild training) and decreased thermal area (TA) were identified as potential sources of cytokine suppression. To explore the effect of acclimation, C57/BL6 mice (n=6) did not receive enrichment or acclimation prior to EHS. Interestingly, exercise acclimation sessions clearly increased the circulating concentrations of IP‐10, KC, MCP‐1, and MIP‐1β (P<0.05), but had no effect on other cytokines. Typical EHS mice experience a TA of »146 (°C x minutes), whereas mice exposed to a “classic” PHS model are exposed to a TA of 409 (°C x min). To control for the influence of the duration of heat exposure, six mice underwent PHS at elevated ambient temperature, designed to match the TA in EHS. Circulating cytokines in this accelerated PHS experiment were similar to classic PHS and did not resemble EHS. In conclusion, shortened thermal area does not account for altered cytokine responses in EHS. However, exercise acclimation changes the magnitude of specific cytokine responses to EHS. This effect may have implications for the positive effects of exercise conditioning or stress reduction on the incidence of heat illness.